Endovascular Intracranial Micro-Catheter Placement to Treat Cavernous SinusThrombosisShahid M Nimjee*, Honey Jones, Sankalp Gohkale, Carmen Graffagnino, Ali R Zomorodi and Tony P Smith

Department Neurological surgery, The Ohio State University Wexner Medical Center, USA

*Corresponding author: Shahid M Nimjee, Department Neurological surgery, The Ohio State University Wexner Medical Center, N-1014 Doan Hall 410 W. 10th Avenue

Columbus, OH 43235, USA; E-mail: shahid.nimjee@osumc.edu

Received date: July 24, 2015; Accepted date: August 25, 2015; Published date: August 29, 2015

Copyright: ©2015 Nimjee SM et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricteduse, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Cavernous sinus thrombosis (CST) is a rare disease that can have devastating morbidity. Despite medicaltherapy, in rare circumstances, patients will continue to decline. We present a patient who complained of headache,left eye pain and vision loss. Magnetic resonance imaging revealed bilateral superior ophthalmic vein and cavernoussinus thrombosis. She was treated with antibiotics and intravenous heparin. Despite a therapeutic activated partialthromboplastic time, she progressed to bilateral blindness. Microcatheter transvenous pharmacological thrombolysiswith recombinant tissue plasminogen activator (rTPA) was performed including overnight continuous infusion. Sherecovered light perception the following morning and left the hospital neurologically intact. This case demonstratesthat in patients with cerebral deep venous thrombosis that decline despite medical therapy, endovascularintervention is a viable option.

Keywords: Cavernous sinus; Superior ophthalmic vein; Thrombus;Endovascular; rTPA

BackgroundCavernous sinus thrombosis (CST) is a rare disease that can have

devastating morbidity. The standard treatment for CST is antibioticsand possibly systemic anticoagulation. Despite medical therapy,patients can continue to decline. We present a patient who presentedwith CST. She was treated with antibiotics and intravenous heparin.Despite a therapeutic activated partial thromboplastic time, sheprogressed to bilateral blindness, confusion and lethargy. We describeendovascular intervention and thrombolysis, resulting in rapid returnof eyesight and baseline neurological function. We also provide a briefoverview CST including causes, diagnosis and current treatment.

Case PresentationA 71-year-old female with a history of chronic sinusitis complained

of worsening headache for a week prior to presentation. She wasprescribed antibiotics. Two days later she awoke with left eye pain,proptosis and decreased vision. She presented to an outside hospitaland was diagnosed with bilateral cavernous sinus thrombosis bymagnetic resonance imaging (MRI). Blood cultures revealed gram-positive cocci. Medical treatment included Vancomycin, Zosyn and acontinuous infusion of heparin. Despite therapeutic levels by activatedpartial thromboplastin time (aPTT), she continued to deteriorateneurologically and was transferred to our facility.

On physical examination she moaned but answered yes or no toquestions. She followed commands in all four extremities. She had leftgreater than right eye chemosis and proptosis with complete ptosis ofleft eye and near-complete of the right (Figure 1A). There were noextra-ocular movements and she was blind in her left eye and couldonly perceive light in the right.

Figure 1: Picture of patient’s eyes A. Before intervention afterantibiotics and anticoagulation had commenced B. Seven days afterintervention.

TreatmentThe right common femoral artery was percutaneously accessed with

a micro puncture device and a 5 French introducer sheath was placed.The patient received a bolus of 3000 units of heparin intravenously(IV) and then continued a titrated dose of 2000 units per hour. HeraPTT was 72.7 seconds while on 2000 units per hour.

A cerebral arteriogram was performed, which demonstratedbilateral cavernous sinus thrombosis and left greater than rightsuperior ophthalmic vein thrombosis (Figure 2). The right and left

Neurology & Neurophysiology

Nimjee SM et al., J Neurol Neurophysiol 2015, 6:4 DOI: 10.4172/2155-9562.1000309

Case Report Open Access

J Neurol NeurophysiolISSN:2155-9562 JNN, an open access journal

Volume 6 • Issue 4• 1000309

Journal of Neurology & Neurophysiology

Jour

nal o

f Neu

rology & Neurophysiology

ISSN: 2155-9562

femoral veins were then percutaneously accessed with a micropuncture device and a 6 French introducer sheath was placed.

Figure 2: Digital subtraction angiography (DSA) of the venousphase from the left common carotid artery (LCCA) demonstratingpatency of venous sinuses and occlusion of superior ophthalmicvein and cavernous sinus. A. Anterior-posterior and B. lateral. Thelarge arrow points towards a void demonstrating no opacificationof the cavernous sinus. The small arrow points towards a voiddemonstrating no opacification of the left superior ophthalmicvein.

A 6 French supporting catheter (Envoy XB, Cordis Inc. MiamiLakes, Florida, USA) was advanced from the right femoral vein intothe right internal jugular vein over a 0.035 inch hydrophilic guidewire(Glidewire, Terumo Medical Corp., Somerset New Jersey, USA). A 2tip micro catheter (Renegade, Boston Scientific Corp. Natick,Massachusetts, USA) was advanced into the right cavernous sinus andright superior ophthalmic vein over a 0.014 inch guidewire (Synchro 2,Stryker Neurovascular, Fremont, California, USA). A right superiorophthalmic vein venogram confirmed thrombosis.

A 6 French Envoy supporting catheter was advanced from the leftfemoral vein into the left internal jugular and an identical 2 tip microcatheter was advanced over a series of micro wires (Synchro 2 andSynchro Standard, Stryker Neurovascular; Glidewire Gold, TerumoMedical Corp.) into the left cavernous sinus. A left cavernous sinusvenogram again confirming thrombosis. Both microcatheters wereconnected to a continuous infusion system and recombinantthromboplatin activatior (rtPA) (Alteplase, Genetech USA Inc., SouthSan Francisco, California, USA) was administered through the microcatheter as a bolus dose of 4 mg (2 mg/microcatheter) followed by a 1mg per hour infusion (.5 mg/catheter) (Figure 3). The heparin wasstopped while the rTPA was being infused.

Figure 3: Intraprocedural DSA images of the micro catheter tipposition in A. Left superior ophthalmic vein and B. right cavernoussinus.

Outcome and Follow upThe following morning, the patient’s vision improved to the point

that she could correctly identify objects in her right eye and had lightperception in the left. Computerized tomography (CT) of the brainwas performed the following morning demonstrating no evidence ofintracranial hemorrhage. All catheters were removed and the IVheparin restarted.

Otolaryngology, head and neck surgery was consulted andrecommended endonasal exploration. Surgery revealed sinus erosionconsistent with multiple bacterial infections. Two biopsy specimenswere consistent with infectious etiology with no evidence ofmalignancy.

Infectious disease was consulted. They recommended continuedantibiotics while in the hospital followed by 3 weeks of intravenousNafcillin and added Moxifloxacin to cover gram-negative bacteria andanaerobes given the intraoperative inflammation seen.

Hematology was consulted. They recommended therapeuticlovenox for 12 months given the potential interaction of the antibioticswith warfarin.

She was discharge after 7 days with a normal neurological exam.Her vision was 20/20 bilaterally with near-complete resolution of herproptosis (Figure 1B). Her extra-ocular movements were intact. Tenmonths after treatment, her vision continues to be intact with no newheadaches or infections.

DiscussionCavernous sinus thrombosis (CST) is a rare pathological

manifestation generally seen in aseptic patients who have hadendonasal surgery or other trauma or in patients with an infectioussource including sinusitis, otitis, odontogenic basis, as well as otherinfections of the face [1]. The pathophysiology behind thedevelopment of CST involves inflammatory changes from regionalinfection of the eyes generating pathological thrombosis, affecting theangular veins. This then invades the superior ophthalmic veins anddirectly spreads to the cavernous sinus. It presents with headache,vision changes, chemosis and proptosis. Cranial nerve symptoms,especially III and VI are hallmarks of progression. Imaging studies fordiagnosis are most often CT venogram and MR venogram. In cases

Citation: Nimjee SM, Jones H, Gohkale S, Graffagnino C, Zomorodi AR, et al. (2015) Endovascular Intracranial Micro-Catheter Placement toTreat Cavernous Sinus Thrombosis. J Neurol Neurophysiol 6: 309. doi:10.4172/2155-9562.1000309

Page 2 of 3

J Neurol NeurophysiolISSN:2155-9562 JNN, an open access journal

Volume 6 • Issue 4• 1000309

where clinical suspicion exists yet conservative imaging is uncertain,digital subtraction angiography can be useful [1].

Therapy for CST includes endonasal exploration and antibioticsin cases where infection is suspected [2,3]. Systemic anticoagulationtherapy is employed but their use has never been adequately studiedgiven the rarity of CST [2]. This particular case represents an instancewhere medical therapy was instituted and the patient continued todecline. Overnight infusion of rTPA within the clot allowed durablethrombolysis to occur and conversion to therapeutic anticoagulationprevented re-thrombosis, over the course of 1- year follow up. Othershave reported endovascular occlusion to treat increased intraocularpressure associated with CST [4]. Our description of endovascularintervention was based on previous experience with treating duralvenous sinus thrombosis (DVST) where a patient declinedneurologically despite maximal medical therapy [5]. As in this case,the patient’s neurological exam improved rapidly followingendovascular thrombolysis. As opposed to the case report where thepatient’s vision improved with endovascular superior ophthalmic veinover the course of 4 months[4], our patient’s visual complaintsresolved in 7 days.

The potential major risk of endovascular intervention ishemorrhage. Given the patient’s precipitous decline and after

obtaining full consent from the family, we felt this was the onlytreatment option to avoid significant morbidity.

In conclusion, endovascular treatment of CST is a reasonableoption in patients who decline neurologically despite medicalmanagement.

References1. Desa V, Green R (2012) Cavernous sinus thrombosis: current therapy.

Journal of oral and maxillofacial surgery: official journal of the AmericanAssociation of Oral and Maxillofacial Surgeons 70: 2085-2091.

2. Bhatia K, Jones NS (2002) Septic cavernous sinus thrombosis secondaryto sinusitis: are anticoagulants indicated? A review of the literature. Seecomment in PubMed Commons below J Laryngol Otol 116: 667-676.

3. Lizé F, Verillaud B, Vironneau P, Blancal JP, Guichard JP, et al. (2015)Septic cavernous sinus thrombosis secondary to acute bacterial sinusitis:a retrospective study of seven cases. Am J Rhinol Allergy 29: e7-12.

4. Ladner TR, Davis BJ, He L, Mawn LA, Mocco J (2014) Transorbitalsuperior ophthalmic vein sacrifice to preserve vision in ocularhypertension from aseptic cavernous sinus thrombosis. J NeurointervSurg .

5. Nimjee SM, Powers CJ, Kolls BJ, Smith T, Britz GW, et al. (2011)Endovascular treatment of venous sinus thrombosis: a case report andreview of the literature. J Neurointerv Surg 3: 30-33.

Citation: Nimjee SM, Jones H, Gohkale S, Graffagnino C, Zomorodi AR, et al. (2015) Endovascular Intracranial Micro-Catheter Placement toTreat Cavernous Sinus Thrombosis. J Neurol Neurophysiol 6: 309. doi:10.4172/2155-9562.1000309

Page 3 of 3

J Neurol NeurophysiolISSN:2155-9562 JNN, an open access journal

Volume 6 • Issue 4• 1000309